ArticleGenes, brain, and behavior2017
Magel2 knockout mice manifest altered social phenotypes and a deficit in preference for social novelty.
Article in Genes, brain, and behavior, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 54 citations in OpenAlex.
- SMCHD1 is a target for gene activation therapy to treat Prader-Willi syndrome.Science advances · 2026Article
- Neonatal social communication and single genes predict the variability of post-pubertal social behavior in a mouse model of paternal 15q11-13 duplication.Research square · 2026Article
- In-depth behavioral characterization of a rat model of Schaaf-Yang syndrome.Scientific reports · 2025Article
- Restoration of NEXMIF expression rescues abnormalities in gene transcription, neuron maturation and autistic-like behaviors in Nexmif knockout mice.Translational psychiatry · 2025Article
- Impaired vasopressin neuromodulation of the lateral septum leads to social behavior deficits in Shank3BNature communications · 2025Article
- Mom genes and dad genes: genomic imprinting in the regulation of social behaviors.Epigenomics · 2025Review
- Investigation of a mouse model of Prader-Willi Syndrome with combined disruption of Necdin and Magel2.JCI insight · 2025Article
- Environmental Enrichment Normalizes Metabolic Function in the Murine Model of Prader-Willi Syndrome Magel2-Null Mice.Endocrinology · 2025Article
- MAGEL2 (patho-)physiology and Schaaf-Yang syndrome.Developmental medicine and child neurology · 2025Review
- Article
- Sex differences in MAGEL2 gene promoter methylation in high functioning autism - trends from a pilot study using nanopore Cas9 targeted long read sequencing.BMC medical genomics · 2024Article
- Neuropeptide therapeutics to repress lateral septum neurons that disable sociability in an autism mouse model.Cell reports. Medicine · 2024Article
- Disengagement of somatostatin neurons from lateral septum circuitry by oxytocin and vasopressin restores social-fear extinction and suppresses aggression outbursts in Prader-Willi syndrome model.Biological psychiatry · 2024Article
- Hormonal Imbalances in Prader-Willi and Schaaf-Yang Syndromes Imply the Evolution of Specific Regulation of Hypothalamic Neuroendocrine Function in Mammals.International journal of molecular sciences · 2023Review
- Glutamatergic cerebellar neurons differentially contribute to the acquisition of motor and social behaviors.Nature communications · 2023Article
- Preimplantation Genetic Testing (PGT) and Prenatal Diagnosis of Schaaf-Yang Syndrome: A Report of Three Families and a Research on Genotype-Phenotype Correlations.Journal of clinical medicine · 2023Article
- Magel2 truncation alters select behavioral and physiological outcomes in a rat model of Schaaf-Yang syndrome.Disease models & mechanisms · 2023Article
- Hypothalamic AAV-BDNF gene therapy improves metabolic function and behavior in theMolecular therapy. Methods & clinical development · 2022Article
- Linking oxytocin and arginine vasopressin signaling abnormalities to social behavior impairments in Prader-Willi syndrome.Neuroscience and biobehavioral reviews · 2022Review
- Next Steps in Prader-Willi Syndrome Research: On the Relationship between Genotype and Phenotype.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
MAGEL2 is one of five protein-coding, maternally imprinted, paternally expressed genes in the Prader-Willi syndrome (PWS)-critical domain on chromosome 15q11-q13. Truncating pathogenic variants of MAGEL2 cause Schaaf-Yang syndrome (SHFYNG) (OMIM #615547), a neurodevelopmental disorder related to PWS. Affected individuals manifest a spectrum of neurocognitive and behavioral phenotypes, including intellectual disability and autism spectrum disorder (ASD). Magel2 knockout mice carrying a maternally inherited, imprinted wild-type (WT) allele and a paternally inherited Magel2-lacZ knock-in allele, which abolishes endogenous Magel2 gene function, exhibit several features reminiscent of the human Prader-Willi phenotypes, including neonatal growth retardation, excessive weight gain after weaning and increased adiposity in adulthood. They were shown to have altered circadian rhythm, reduced motor activity and reduced fertility. An extensive assessment for autism-like behaviors in this mouse model was warranted, because of the high prevalence of ASD in human patients. The behavior of Magel2 knockout mice and their WT littermates were assayed via open field, elevated plus maze, tube, three-chamber and partition tests. Our studies confirm decreased horizontal activity of male and female mice and increased vertical activity of females, in the open field. Both sexes spent more time in the open arm of the elevated plus maze, suggestive of reductions in anxiety. Both sexes displayed a lack of preference for social novelty, via a lack of discrimination between known and novel partners in the partition test. The in-depth investigation of behavioral profiles caused by Magel2 loss-of-function helps to elucidate the etiology of behavioral phenotypes both for SHFYNG and PWS in general.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.